Exercise hyperemia in potassium-depleted dogs.

The experiments reported here are designed to evaluate the role of potassium (K+) in exercise hyperemia. Desoxycorticosterone acetate was implanted subcutaneously in six dogs, which were then placed on K+-deficient diets. Experiments were performed 3 or 4 wk later. Exercise vasodilation was much reduced in K+-depleted animals. However, when muscle stimulation caused very little vasodilation (i.e., in the most depleted animals) the muscle also produced little tension and extracted very little O2. O2 extraction was not limited by O2 availability. When the change in vascular resistance was plotted against O2 extraction, the data from K+-depleted dogs fell on a line constructed for control dogs. We conclude that the reduced exercise hyperemia of K+-depleted dogs is a result of reduced muscle O2 consumption rather than decreased K+ release. However, there was reduced vasodilation in response to brief tetanus and a loss of the triphasic initiation of exercise vasodilation with twitch work. This suggests that absence of K+ release does directly affect initiation of exercise vasodilation.